Specific objectives are to define principal mechanisms of cellular uptake of carcinogens in plasma lipoproteins. There may be (a) passive transfer of polynuclear aromatic hydrocarbons (PAH) from plasma lipoproteins to cultured endothelial cells, (b) lipoprotein lipase dependent transfer of PAH in triglyceride-rich lipoproteins to endothelial cells, and (c) cellular uptake of lipoproteins containing PAH. The general objective is to determine if PAH entry into cells is controlled by thermodynamics or by the kinetics of lipoprotein modification and endocytosis. Specific hypotheses are these: (1) At the cell surface, lipoprotein lipase action will reduce lipoprotein size and change the composition of the lipoprotein surface film. PAH may then be transferred by either or both of the following mechanisms: (a) by lateral movement through an interfacial continuum formed by fusion, (b) as individual molecules through the aqueous solution. (2) PAH in low density lipoproteins and in triglyceride-poor remnants are internalized by several endocytotic processes. The initial step of chemical carcinogenesis is delivery of the carcinogen to the target tissue. In plasma, nonpolar substances such as PAH are confined to plasma lipoproteins. Transport of PAH has a regulatory role as a rate determining step. Evaluation of the mechanisms of transfer, of the rates of competitive processes, and of the thermodynamics of distribution of PAH and their metabolites is necessary to understand the relationship of carcinogenesis and lipid metabolism.